Acute spinal cord ischemia syndrome (ASCIS) comprises only 1.2% of all strokes and most frequently involves the anterior spinal cord artery territory. Cocaine use in young adults is well known to be responsible for acute ischemic strokes in individuals who lack other vascular risk factors. Here we present a rare case of cocaine-induced ASCIS as the etiology of nontraumatic acute spinal cord myelopathy. 

Our patient was a 40-year-old female, who presented with acute-onset bilateral lower extremity weakness, sensory loss, neck pain, and bladder incontinence. She had history of intravenous drug use of crack-cocaine prior to symptoms, confirmed on urine drug screen. She had no other vascular risk factors, preceding trauma, recent infections/vaccinations, or travel history. MRI neuroaxis showed two areas of non-enhancing contiguous T2-hyperintensities from C5-C6 and T4 to the conus with cord expansion. Extensive workup for other etiologies of non-traumatic myelopathy was completed and unremarkable. The patient completed 5 days of plasma exchange without clinical improvement. 

While cocaine-induced cerebrovascular events are well documented, very few cases of cocaine-related ASCIS have been described. These cases have all involved young adults between 20-40 years old, with rapid initial onset of symptoms. Clinical presentation varies depending on the involved vascular territory. MRI findings of ASA infarcts show “pencil-like” lesions on T2-sagittal MRI images or an “owl’s eye” appearance on T2-axial imaging as was seen in our patient. The mechanism of stroke is thought to be multifactorial due vasospasm, vascular thrombosis, cardioembolism, or hypertensive surges. Given the scarcity of these events, previous patient outcomes of cocaine-related ASCIS are unclear. Studies have shown that ASIA Impairment Scale score, lesion level, and patient age were the strongest predictors of neurologic and functional outcomes, whereas etiology of the ischemia had no effect on outcomes.